The correlation between IGF-II and Bcl-2 expression in colorectal adenocarcinoma.

Med Oncol

Department of Oncology, Tongji Hospital, Huazhong University of Science and Technology, 1095 Jiefang Road, Wuhan 430030, China.

Published: June 2012

Our aim for this study was to investigate the correlation and clinical significance between the expression of IGF-II and Bcl-2 in colorectal adenocarcinoma, especially in terms of the metastasis of colorectal adenocarcinoma. Sixty paraffin embedded samples of colorectal adenocarcinoma were selected, and fifteen normal colorectal tissues were used as controls. IGF-II mRNA was detected using in situ hybridization, and the expression of Bcl-2 along with the proliferating cell nuclear antigen (PCNA) protein was detected through immunohistochemistry. The TUNEL assay was used to detect apoptosis. Specimens with a positive cell ratio less than 30% were defined as negative. The levels of IGF-II mRNA and the Bcl-2 protein were significantly higher in colorectal adenocarcinoma (39.64 ± 7.38% and 30.74 ± 7.22%, respectively) than in normal colorectal tissues (22.56 ± 4.21% and 12.17 ± 1.94%, respectively) (P < 0.01). The levels were related to Dukes' stage and lymph node metastases, but were unrelated to patient age, gender, tumor site, tumor size, and tumor differentiation. Also, a negative correlation was observed between IGF-II mRNA and Bcl-2 protein (P < 0.05) during Dukes' stages. In addition, a positive correlation between IGF-II mRNA and PCNA or apoptosis, as well as a negative correlation between Bcl-2 and apoptosis were observed (P < 0.01). There was no correlation between Bcl-2 and PCNA (P > 0.05). The patients detected as IGF-II mRNA (+) and Bcl-2 (-) showed the worst prognosis. The expression of IGF-II and Bcl-2 was correlated with the clinical manifestation of colorectal adenocarcinoma; thus, the assessment of both IGF-II and Bcl-2's status will provide important information regarding the diagnosis and prognosis of colorectal adenocarcinoma.

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http://dx.doi.org/10.1007/s12032-011-9881-4DOI Listing

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